ArticleScientific reports2017
RNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Dynamic Gene Expression Signatures across Stages of Carotid Plaque Calcification.Journal of vascular research · 2026Article
- Mechanisms of Cardiovascular Calcification and Experimental Models: Impact of Vitamin K Antagonists.Journal of clinical medicine · 2024Review
- NSUN6 and HTR7 disturbed the stability of carotid atherosclerotic plaques by regulating the immune responses of macrophages.Open medicine (Warsaw, Poland) · 2024Article
- Hua-Feng-Dan Alleviates LPS-induced Neuroinflammation by Inhibiting the TLR4/Myd88/NF-κB Pathway: Integrating Network Pharmacology and Experimental Validation.Current pharmaceutical design · 2024Article
- Transcriptomic research in atherosclerosis: Unravelling plaque phenotype and overcoming methodological challenges.Journal of molecular and cellular cardiology plus · 2023Review
- Vascular smooth muscle cell phenotype switching in carotid atherosclerosis.JVS-vascular science · 2022Article
- Inflammation, Oxidative Stress, Senescence in Atherosclerosis: Thioredoxine-1 as an Emerging Therapeutic Target.International journal of molecular sciences · 2021Review
- Efficacy of simvastatin on carotid atherosclerotic plaque and its effects on serum inflammatory factors and cardiocerebrovascular events in elderly patients.Experimental and therapeutic medicine · 2021Article
- Modular genome-wide gene expression architecture shared by early traits of osteoporosis and atherosclerosis in the Young Finns Study.Scientific reports · 2021Article
- Novel Transcript Discovery Expands the Repertoire of Pathologically-Associated, Long Non-Coding RNAs in Vascular Smooth Muscle Cells.International journal of molecular sciences · 2021Article
- Targeting non-coding RNAs in unstable atherosclerotic plaques: Mechanism, regulation, possibilities, and limitations.International journal of biological sciences · 2021Review
- Weighted Gene Co-expression Network Analysis Identifies Crucial Genes Mediating Progression of Carotid Plaque.Frontiers in physiology · 2021Article
- Article
- Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis.European heart journal · 2020Article
- Vascular smooth muscle cells in atherosclerosis.Nature reviews. Cardiology · 2019Review
- Transcriptomics of Human Arteriovenous Fistula Failure: Genes Associated With Nonmaturation.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2019Article
- Article
- Endothelial prostaglandin DJournal of the renin-angiotensin-aldosterone system : JRAASArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carotid artery atherosclerosis is a risk factor to develop cerebrovascular disease. Atheroma plaque can become instable and provoke a cerebrovascular event or else remain stable as asymptomatic type. The exact mechanism involved in plaque destabilization is not known but includes among other events smooth muscle cell (SMC) differentiation. The goal of this study was to perform thorough analysis of gene expression differences in SMCs isolated from carotid symptomatic versus asymptomatic plaques. Comparative transcriptomics analysis of SMCs based on RNAseq technology identified 67 significant differentially expressed genes and 143 significant differentially expressed isoforms in symptomatic SMCs compared with asymptomatic. 37 of top-scoring genes were further validated by digital PCR. Enrichment and network analysis shows that the gene expression pattern of SMCs from stable asymptomatic plaques is suggestive for an osteogenic phenotype, while that of SMCs from unstable symptomatic plaque correlates with a senescence-like phenotype. Osteogenic-like phenotype SMCs may positively affect carotid atheroma plaque through participation in plaque stabilization via bone formation processes. On the other hand, plaques containing senescence-like phenotype SMCs may be more prone to rupture. Our results substantiate an important role of SMCs in carotid atheroma plaque disruption.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.